Association Between Oxidative Damage Markers and Self-Reported Temporomandibular Dysfunction Symptoms in Patients with Chronic Fatigue Syndrome

Abstract

Full blood counts, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), haematinics and markers for oxidative stress were measured on thirty-three patients diagnosed with chronic fatigue Ross S. Richards is Faculty syndrome (CFS) and twenty-seven age and sex matched controls. The CFS patients had increased prevalence of symptoms of temporomandibular dysfunction (TMD). Jaw muscle pain was associated with increases in methaemoglobin (P < .002), ferritin (P < .02) and malondialdehyde (P < .007) whilst temporomandibular joint (TMJ) clicking and/or locking was associated with increases in methaemoglobin (P < .001), malondialdehyde (P < .05) and vitamin B 12 (P < .02) levels. Multiple regression analysis found methaemoglobin to be the principle component associated with TMD symptoms in the CFS patients. Increases in scalar severity responses to jaw muscle pain and TMJ clicking and/or locking were positively correlated with methaemoglobin by multiple regression. These data indicate that oxidative stress due to excess free radical formation was associated with jaw muscle pain in CFS patients and suggest that these symptoms were likely to be associated with a pathogen-associated aetiology.

Changes in the salivary oxidative status in individuals with temporomandibular disorders and pain

“…5 On the other hand, Nitzan et al 29 stated that increased oxidative stress caused by free radicals in the TMJ could cause the imbalance of local antioxidant defences, deteriorating joint lubrication. Richards et al 30 evaluated blood oxidative stress in individuals with temporomandibular dysfunction who also suffer from chronic fatigue syndrome, and observed an association between increased levels of oxidative stress and total free radicals. These patients felt a great deal of pain in the masticatory muscles.…”

“…These patients felt a great deal of pain in the masticatory muscles. 30 A lower TAC suggests that the imbalance in antioxidant mechanisms can influence pain mechanisms in TMDs, characterized by an insufficient response against oxidative stress caused by free radicals. TOS values were similar in both groups suggesting that changes related to the TAC in TMDs with pain can be considered a major determinant factor when compared to oxidative stress.…”

Evidence of oxidative stress in temporomandibular disorders: a pilot study

“…It is possible that the mechanical stress of both TMJ and masticatory muscles can generate FR through a number of mechanisms, triggering a cascade of reactions that can exacerbate tissue damage, inflammation and pain (6). An accumulation of FR in the joint can occur from mechanical strain, internal derangements and injury of the joint tissues that can overwhelm the local antioxidant defences resulting in protective peripheral nociception and reactive degeneration (2, 6, 12).…”

“…Temporomandibular muscle and joint disorders (TMJD) are characterised by persistent jaw pain associated with dysfunction and tenderness of the temporomandibular muscles and joints (1). Biomarkers have been studied in patients with TMJD to elucidate the mechanisms of pain and provide a basis for early detection of pain and degeneration and a potential target for therapeutic agents to prevent progression to more severe pain and dysfunction (2–10). Biomarkers of oxidative stress (OS) have been found significant higher in serum of rats in IL‐1α‐induced TMJ arthritis by Kawai and colleagues (2000) (11).…”

The evaluation of oxidative stress and inflammation markers in serum and saliva of the patients with temporomandibular disorders

“…It is possible that mechanical stress in the TMJ and masticatory muscles can produce free radicals through a number of mechanisms that exacerbate tissue damage, inflammation, and pain [ 18 ]. Free radical accumulation in the joint may occur with mechanical tension suppressing the local antioxidant defense, internal irregularities, and damage to the joint tissues [ 18 – 20 ]. It is known that hypoxia damage caused by repeated strain on the muscles can increase the formation of free radicals and pain inflammatory mediators [ 21 ].…”